Repetition of skin damage and regeneration due to ultraviolet (UV) light of sun light forms wrinkles, which leads to “photo-aging”. Chronic exposure to UV light increases expression of matrix metalloproteinases (MMPs) and destroys collagen corresponding to an extracellular matrix (ECM) protein which is important in elasticity and strength of the skin tissue while occupying 80% or more of the dermis layer. The destroyed collagen is accumulated in a deformed form during the process of wound healing, resulting in the formation of clinical wrinkles. Further, continuous exposure of the skin to UV light increases secretion of inflammatory cytokines, thereby causing chronic skin inflammatory response.
Meanwhile, adiponectin, a representative adipokine secreted in adipocytes, is known to have functions of as lipogenesis and lipolysis, regulation of the appetite, insulin resistance, and inflammation, etc. Recently, researches have shown that adiponectin is decreased in the subcutaneous adipocytes of the photo-aged skin. It has been reported that decreasing expression of adiponectin by UV light accelerates photo-aging by increasing MMP-1 and inhibiting collagen biosynthesis.
Further, autophagy is a mechanism to regenerate energy and remove damaged materials by degradingaged or damaged intracellular materials and organelles in cells when an energy source in the cells is exhausted or stress factors in cells are excessively generated, and autophagy enables maintenance of normal cells. In addition to maintain intracellular homeostasis, autophagy is also involved in immune cell responses and inflammatory pathway. Mechanism for removing microorganisms in cells is provided through autophagy acceptors.
Recently, in various studies, it was reported that as the aging has proceeded or been accelerated, the autophagy activity in cells has rapidly decreased. Further, in the case of suppressing the autophagy, aged mitochondria, misfolded proteins, or the like, are excessively accumulated in cells, such that free radicals and oxidative stress in the cells are increased, thereby resulting in increasing apoptosis and promoting aging. Therefore, denatured proteins, lipid, mitochondria, and the like, may be rapidly removed by activating autophagy mechanism to decompose aged materials and organelles in cells and reuse decomposed products, such that an environment in which cells may live in a healthier state may be provided.
Therefore, it is expected that in the case of developing a novel active material capable of promoting autophagy activation in cells while increasing expression of adiponectin, the damaged skin of wrinkles due to UV light, toxic substances caused by oxidative stress and micro inflammatory environment will be recovered, thereby preventing photo-aging.
The disclosure of this section is to provide background of the invention. Applicant notes that this section may contain information available before this application. However, by providing this section, Applicant does not admit that any information contained in this section constitutes prior art.